There are many documents reporting that chromosome instability is involved in development of a cancer. In addition, it has been recently demonstrated that a defect in a molecule controlling a checkpoint during the G2/M phase in a cell cycle causes chromosome instability. However, since in many carcinoma cells, a gene defect in a molecule controlling a checkpoint in the cell is not frequently observed, a mechanism of inducing chromosome instability, which is substantially involved in onset of the cancer, remains still unclear in many aspects. types of HPV-16 or HPV-18. In a cervical cancer tissue, HPV infection has been observed at a frequency of 90% or more. In a development mechanism of cervical cancer induced by HPV infection, E6 and E7 gene products of the virus play an important role. Specifically, it is known that E6 accelerates a process for digesting p53 tumor suppressor protein, while E7 blocks canceration-inhibiting activity of pRB (retinoblastoma) tumor suppressor protein that is a Rb gene product, which two steps result in tumorigenesis. A specific oncogenic protein activated by HPV infection has not, however, been identified yet. Particularly, E6 and E7, viral gene products of HPV, induce chromosome instability and characterize a cell, but detail of its mechanism directly related there to is left substantially unknown in variety of aspects. For approaching to treatment of cervical cancer, it is, therefore, very important to identify an oncogenic protein as a target for HPV and an encoding oncogene thereof. Cervical cancer progresses from a precancerous state, i.e., dysplasia (epithelial dysplasia of cervical squamous cell) to invasive cancer. Depending on a case, the disease may remain in the dysplasia stage without progressing to cancer. On the other hand, there are considerable cases where dysplasia may rapidly progress to an advanced cancer. In view of the situation, it may be important for more accurate cancer diagnosis to identify a molecule directly involved in development of cervical cancer.